Chronic stress has been linked to hypertension, but the underlying mechanisms remain poorly specified. We suggest that chronic stress poses a risk for hypertension through repeated occurrence of acute stressors (often stemming from the chronic stress context) that cause activation of stress-mediating physiological systems. Previous models have often focused on the magnitude of the acute physiological response as a risk factor; we attempt to extend this to address the issue of duration of exposure. Key to our model is the notion that these acute stressors can emerge not only in response to stressors present in the environment, but also to mental representations of those (or other) stressors. Consequently, although the experience of any given stressor may be brief, a stressor often results in a constellation of negative cognitions and emotions that form a mental representation of the stressor. Ruminating about this mental representation of the stressful event can cause autonomic activation similar to that observed in response to the original incident, and may occur and persist long after the event itself has ended. Thus, rumination helps explain how chronic stress causes repeated (acute) activation of one's stress-mediating physiological systems, the effects of which accumulate over time, resulting in hypertension risk.
All Science Journal Classification (ASJC) codes
- Internal Medicine